Coccoid Forms of<i>Helicobacter pylori</i>in the Human Stomach

Chan, Wing-Yee; Hui, Pui Wah; Leung, Kai-Man; Chow, John; Kwok, Francis; Ng, Chi-Sing

doi:10.1093/ajcp/102.4.503

Cited by 120 publications

(93 citation statements)

References 14 publications

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“…Coccoid H. pylori maintains the same antigenic characteristics as the bacillary form. 41 In addition, experimental animal models indicate that the coccoid form of H. pylori reverts to the bacillary form and induces gastritis and ulcer. 42 Successful culture of H. pylori from the gastric lymph nodes suggests that some of H. pylori-positive macrophages at the paracortical areas may have carried coccoid forms of H. pylori.…”

Section: Intestinal Metaplasiamentioning

confidence: 99%

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Ito

Kobayashi

Uchida

et al. 2008

Laboratory Investigation

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Helicobacter pylori has been considered to be non-invasive and to rarely infiltrate the gastric mucosa, even though there is an active Th1 immune response in the lamina propria of the H. pylori-infected stomach. To elucidate whether H. pylori invades the lamina propria and translocates to the gastric lymph nodes, we examined H. pylori in formalin-fixed and paraffin-embedded tissue sections of stomach and gastric lymph nodes obtained from 51 cancer patients using real-time PCR and immunohistochemistry (IHC) with a novel anti-H. pylori monoclonal antibody that recognizes lipopolysaccharides. Fresh gastric lymph nodes were used to culture for H. pylori. In 46 patients with H. pylori in the stomach, the bacterium was found in the lymph nodes from 21 patients by culture, 37 patients by PCR, and 29 patients by IHC. H. pylori captured by macrophages was found in the lamina propria of 39 patients. In the lymph nodes, the bacterium was found in many macrophages and a few interdigitating dendritic cells at the paracortical areas. H. pylori was also found in the intracellular canaliculi of parietal cells in 21 patients, but intracytoplasmic invasion into gastric epithelial cells was not identified. When compared to the commercially available anti-H. pylori antibodies, the novel antibody showed the highest sensitivity to detect H. pylori-positive macrophages, whereas no difference was found for H. pylori in the mucous layer. The H. pylori-positive macrophages in the lamina propria correlated with chronic gastritis as well as translocation of such cells to the lymph nodes. These results suggest that H. pylori-induced gastric epithelial damage allows the bacteria to invade the lamina propria and translocate to the gastric lymph nodes, which may chronically stimulate the immune system. The bacteria captured by macrophages, whether remaining alive or not, may contribute to the induction and development of H. pylori-induced chronic gastritis.

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Section: Intestinal Metaplasiamentioning

confidence: 99%

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Ito

Kobayashi

Uchida

et al. 2008

Laboratory Investigation

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“…Growing evidence supports the concept that H. pylori exists in two viable forms, spiral or coccoid, and several studies have shown that the coccoid form cannot be cultured or be detected by RUT or histology but can be detected PCR (Bode et al, 1993;Chan et al, 1994;Hulten et al, 1996;Moayyedi and Dixon, 1998;He et al, 2002). Consequently, another possible explanation for our findings could be a high percentage of the coccoid form of H. pylori as a result of antibiotic treatment in the patients from group B. Additionally, He et al (2002) have suggested the possibility that no viable H. pylori were present in the biopsy sample but only dead bacteria or chromosomal DNA.…”

mentioning

confidence: 93%

Quantitative real-time PCR for the clinical detection of Helicobacter pylori

et al. 2007

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Accurate diagnosis of Helicobacter pylori infection is very important in both clinical practice and research. We evaluated the sensitivity of real-time PCR (RT-PCR) for the detection and quantification of Helicobacter pylori using DNA from 91 human gastric biopsy samples divided into three groups: 46 biopsies from untreated patients who according to the references methods were considered H. pylori-negative (group A); 35 biopsies from patients previously treated against H. pylori and considered to be cured by "gold standard" tests (group B); and 10 biopsies from patients H. pylori-positive by all available methods (group C). The sensitivity of the RT-PCR assay was higher than that of standard methods. Of the 81 patients considered to be uninfected according to the references methods, 16 were H. pylori-positive by PCR, 10 of which were patients who had received H. pylori eradication therapy and 6 were untreated patients. Based on these findings we recommend that RT-PCR should be use in addition to standard methods in clinical studies to monitor the results of H. pylori eradication therapy.

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“…The role of the coccoid form in pathogenesis of H. pylori-associated gastritis has been disputed. Some authors consider the coccoid form as a degenerative or dead form of H. pylori [ 16,21,25], while others consider it as a resting but still metabolic active form [2, 3,12,22,29,321. The aim of this study was to demonstrate the conversion of spiral form of H. pylon to coccoid forms, and to show both degenerative and intact subcellar morphology suggesting that some of the coccoid bacteria may be viable.…”

Section: Introductionmentioning

confidence: 99%

Morphologic Conversion of Helicobacter Pylori from Spiral to Coccoid Form: Scanning (SEM) and Transmission Electron Microscopy (TEM) Suggest Viability

Wïllén¹,

Carlén²,

Wang³

et al. 2000

Upsala Journal of Medical Sciences

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Helicobacter pylon is a pathogen associated with type B gastritis, peptic ulcer disease, gastric atrophy, and stomach cancer. H. pylori exists in two morphological forms, spirals and coccoids. The latter has been described as viable but non-cultivable. The role of the coccoid form in the pathogenesis of gastric disease is disputed. Some authors consider the coccoid form to be a degenerative or dead form of H.pylori, while others consider it a resting but still metabolically active form.This study reports the conversion fiom spiral to coccoid form ultrastructurally. Dense material is accumulated in the periplasmic space, the spiral bacteria bend and the outer membrane is separated from the inner cell wall layer. Remodeling of inner structures takes place, ending in the coccoid form of the bacteria with preserved light polyphosphate areas. Reduction of surface takes place by production of surface membrane vesicles, which later are squeezed off. The finding of preserved subcellular structures +d intact double membranes in combination with degenerative forms suggests that some of the coccoids are viable. Scanning electron microscopy (SEM) demonstrates coccoid form of bacteria with slightly ruffled surfaces but no spiral forms.

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Coccoid Forms ofHelicobacter pyloriin the Human Stomach

Cited by 120 publications

References 14 publications

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Quantitative real-time PCR for the clinical detection of Helicobacter pylori

Morphologic Conversion of Helicobacter Pylori from Spiral to Coccoid Form: Scanning (SEM) and Transmission Electron Microscopy (TEM) Suggest Viability

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